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目的为探讨非小细胞肺癌（ＮＳＣＬＣ）细胞中第三号染色体短臂上３ｐ２５位点上等位基因的杂合性丢失（ＬｏｓｓｏｆＨｅｔｅｒｏｚｙｇｏｓｉｔｙＬＯＨ）与肺癌发生发展的相关性。方法采用银染聚合酶链反应（ＰＣＲ）结合二核苷酸（ＣＡ）ｎ重复程序出现多态性评价杂合性丢失方法，分析５８例ＮＳＣＬＣ组织中３ｐ２５等位基因的杂合性丢失。结果５８例肺癌组织中有２９例出现３ｐ２５ＬＯＨ，总的杂合性丢失率为５０％。３ｐ２５的杂合性丢失率在１８例腺癌中为１２例（６６．７％），明显高于鳞癌（４２．９％，１５／３５），有显著性统计学意义（Ｐ＜０．０５），但３ｐ２５杂合性丢失与ＮＳＣＬＣ临床分期关系不明显，Ⅰ期为４２．１％，Ⅱ期为５５．６％和Ⅲ期为５２．２％，５例正常胎儿肺组织均不出现３ｐ２５ＬＯＨ。结论３ｐ２５杂合性丢失在ＮＳＣＬＣ中普遍存在，从而说明３ｐ２５位点处存在着某些与肺癌发生发展有关的抑癌基因。
Objective To investigate the association between Loss of Heterozygosity (LOH) at the 3p25 locus and the development of lung cancer in non-small cell lung cancer (NSCLC) cells. Methods The heterozygosity loss was evaluated by polymorphism of silver staining polymerase chain reaction (PCR) combined with dinucleotide (CA) n repeat procedure. The loss of heterozygosity of 3p25 allele was analyzed in 58 cases of NSCLC. Results Of the 58 lung cancers, 29 showed 3p25LOH, and the total loss of heterozygosity was 50%. Loss of heterozygosity at 3p25 in 12 cases of adenocarcinoma (66.7%) was significantly higher than that of squamous cell carcinoma (42.9%, 15/35), with statistical significance (P<0. 05), but the loss of heterozygosity at 3p25 was not significantly associated with the clinical stage of NSCLC, 42.1% at stage I, 55.6% at stage II, and 52.2% at stage III. None of the five normal fetal lung tissues appeared 3p25LOH. Conclusion Loss of heterozygosity at 3p25 is common in NSCLC, indicating that there are some tumor suppressor genes associated with the development of lung cancer at the 3p25 site.